The polymerization of sickle hemoglobin results in the clinical manifestations of sickle cell disease. Dehydrated cells result from repeated sickling caused by the polymerized sickle cell hemoglobin and are thought to play a major role in vaso-occlusive process. Magnesium can inhibit RBC dehydration and in a sickle cell transgenic mouse model, a high magnesium diet decreased dense cells. Preliminary results from patients enrolled in this trial indicate that despite little change in blood magnesium levels some decrease in the patients' dense calls have been noted by the end of therapy. Because of this delay in response to magnesium the length of time patients will be treated with magnesium will be increased and the dosage will be increased further in the absence of toxicity of hypermagnesemia.